Sinomenine ameliorates collagen-induced arthritis in mice by targeting GBP5 and regulating the P2X7 receptor to suppress NLRP3-related signaling pathways.

Sinomenine (SIN) is an isoquinoline alkaloid isolated from Sinomenii Caulis, a traditional Chinese medicine used to treat rheumatoid arthritis (RA). Clinical trials have shown that SIN has comparable efficacy to methotrexate in treating patients with RA but with fewer adverse effects. In this study, we explored the anti-inflammatory effects and therapeutic targets of SIN in LPS-induced RAW264.

Sinomenine inhibits macrophage M1 polarization by downregulating α7nAChR via a feedback pathway of α7nAChR/ERK/Egr-1.

Background: Sinomenine (SIN) is an anti-inflammatory drug that has been used for decades in China to treat arthritis. In a previous study, SIN acted on α7 nicotinic acetylcholine receptor (α7nAChR) to inhibit inflammatory responses in macrophages, which indicates a new anti-inflammatory mechanism of SIN. However, the level of α7nAChR was increased in the inflammatory responses and was downregulated by SIN in vitro, so the underlying mechanisms of SIN acting on α7nAChR remain unclear.

Alpha7 nAChR Expression Is Correlated with Arthritis Development and Inhibited by Sinomenine in Adjuvant-Induced Arthritic Rats.

Sinomenine (SIN) is the active ingredient of the Chinese herb that has been used to treat rheumatoid arthritis (RA) for about 30 years in China. Marked expression of the alpha7 nicotinic acetylcholine receptor (7nAChR) in the joint synovium of RA patients suggested a relationship between 7nAChR and RA. This study investigated the relationship between 7nAChR and RA development and the effects of SIN on 7nAChR expression and .

Sinomenine regulates CD14/TLR4, JAK2/STAT3 pathway and calcium signal via α7nAChR to inhibit inflammation in LPS-stimulated macrophages.

To investigate the cellular mechanism that sinomenine (SIN) inhibits inflammation in macrophages induced by LPS through α7 nicotinic acetylcholine receptor (α7nAChR). RAW264.7 cells were stimulated with LPS and treated by SIN or nicotine (Nic).

Sinomenine inhibits fibroblast-like synoviocyte proliferation by regulating α7nAChR expression via ERK/Egr-1 pathway.

Fibroblast like synoviocyte (FLS) is a crucial in the pathogenesis of rheumatoid arthritis (RA), and involved in inflammation and joint destruction. Sinomenine (SIN), an alkaloid derived from the plant Sinomenium acutum, has anti-inflammatory and analgesic effect and been used for RA treatment in China. Alpha 7 nicotinic acetylcholine receptors (α7nAChR), as the key receptor in cholinergic anti-inflammatory pathway (CAP) to inhibit inflammation, has been detected in RA patients synovium, but its role is still unclear.

Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis.

Recently, microsomal prostaglandin E synthase 1 (mPGES-1) has attracted much attention from pharmacologists as a promising strategy and an attractive target for treating various types of diseases including rheumatoid arthritis (RA), which could preserve the anti-inflammatory effect while reducing the adverse effects often occur during administration of non-steroidal anti-inflammatory drugs (NSAIDs). Here, we report that sinomenine (SIN) decreased prostaglandin (PG)E levels without affecting prostacyclin (PG)I and thromboxane (TX)A synthesis via selective inhibiting mPGES-1 expression, a possible reason of low risk of cardiovascular event compared with NSAIDs. In addition, mPGES-1 protein expression was down-regulated by SIN treatment in the inflamed paw tissues both in carrageenan-induced edema model in rats and the collagen-II induced arthritis (CIA) model in DBA mice.

α7 Nicotinic Acetylcholine Receptor is a Novel Mediator of Sinomenine Anti-Inflammation Effect in Macrophages Stimulated by Lipopolysaccharide.

Sinomenine (SIN), an alkaloid derived from the plant Sinomenium acutum, has anti-inflammatory and analgesic effects and has been used for rheumatoid arthritis treatment in China. This study aims to verify the hypothesis that SIN acts on α7 nicotinic acetylcholine receptor (α7nAChR) to inhibit the activation of macrophages stimulated by lipopolysaccharide. The prototypical α7nAChR antagonist α-bungarotoxin and mecamylamine attenuated the effect of SIN on tumor necrosis factor-α and interleukin-6 in RAW264.

[Effects of total alkaloids of Tongbiling prescription on Th1 type cytokine expression in T lymphocytes].

Aim: To study the effects of total alkaloid of Tongbiling prescription(TBL) on Th1 type cytokine expression in T cells in order to elucidate the anti-inflammatory mechanism of TBL.

Methods: The lymphocytes were isolated from mouse mesenteric lymph nodes and cultured in-vitro. Various concentrations of TBL were added to the culture followed by phorbol ester and inomycin treatment and then incubated for another 4 hours.

[The effect of sinomenine on cyclooxygenase activity and the expression of COX-1 and COX-2 mRNA in human peripheral monocytes].

Objective: To observe in vitro the effect of Sinomenine, a pure alkaloid extracted from the chinese medical plant Sinomenium acutum on the activity of cyclooxygenase (COX-1 and COX-2) and the expression of COX-1 and COX-2 mRNA.

Method: Mononuclear leukocytes were obtained from healthy adults. Isolated mononuclear leucocytes from human peripheral blood (PBMC) were incubated (1 x 10(6).

[Gene expression of toll-like receptors in the liver, lungs and spleen in mice after endotoxin challenge].

Objective: To investigate the gene expression of some lipopolysaccharide (LPS) receptors after LPS stimulation.

Methods: The total RNA from normal and LPS-challenged mice was extracted by Trizol reagent and the gene expression of Toll-like receptor 2 (TLR2), TLR4, CD(14), LPS-binding protein (LBP) and tumor necrosis factor-alpha(TNF-alpha) were measured by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).

Results: The gene of TLR2 was expressed in normal lungs and spleen tissues, and TLR2, CD(14), LBP in liver.